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Acute administration of 17β-estradiol (E₂) exerts antiatherosclerotic effects in healthy postmenopausal women. The vasoprotective action of E₂ may be partly accounted for by a rapid increase in nitric oxide (NO) levels in endothelial cells (ECs). However, the signaling mechanisms producing this rise are unknown. In an attempt to address the short-term effect of E₂ on endothelial NO production, confluent bovine aortic endothelial cells (BAECs) were incubated in the absence or presence of E₂, and NO production was measured. Significant increases in NO levels were detected after only 5 min of E₂ exposure without a change in the protein levels of endothelial NO synthase (eNOS). This short-term effect of estrogen was significantly blunted by various ligands which decrease intracellular Ca²⁺ concentration. Furthermore, plasma membrane-impermeable BSA-conjugated E₂ (E₂BSA) stimulated endothelial NO …